The CFH Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphoblastoid cell line. These cells feature targeted disruption of the CFH gene, resulting in a loss-of-function model for the key complement regulator factor H. The polyclonal format provides a heterogeneous pool of edited cells, suitable for pooled functional screens and population-level assays.
Raji is an Epstein-Barr virus-positive continuous B lymphocyte line established from a Burkitt??s lymphoma patient. It expresses surface IgM and exhibits characteristics of transformed B cells, making it a standard model for B cell immunology, signal transduction, and viral host interaction studies. Its robust growth and reproducible responses facilitate consistent complement assays.
CFH encodes factor H, a fluid-phase inhibitor of the alternative complement pathway. It binds C3b, accelerates C3 convertase decay, and serves as cofactor for factor I-mediated C3b cleavage, thereby suppressing C3b amplification, C5a generation, and MAC assembly. Expression is induced by IFN-??, TNF-??, and IL-6 through STAT1 and NF-??B. Factor H interacts with C3b, factor I, CRP, and host glycocalyx components. It functionally opposes CFB and CFD and works alongside CD46, CD55, and CD59 to protect cells.
Disruption of CFH in Raji cells abolishes the primary alternative pathway inhibitor, resulting in excessive C3b deposition, heightened C5a and MAC production, and increased complement-mediated lysis. This B cell-specific knockout recapitulates features of aHUS, AMD, and C3 glomerulopathy, enabling dissection of factor H-related pathology and complement-dependent B cell regulation.
Typical assays include flow cytometric measurement of C3b deposition, complement hemolytic assays, ELISA for C3a/C5a, and cell viability under complement attack. Western blot and RT-qPCR confirm CFH knockout and downstream changes. The model supports therapeutic screening for complement inhibitors and factor H structure-function research. Immunofluorescence for MAC and complement-mediated cytotoxicity assays enable detailed mechanistic studies. For further technical information, contact Ascent Research.
